Imaging description

Osmotic myelinolysis (OM) is a distinctive clinical syndrome with classic symptoms of acute mental status change, pseudobulbar palsy, and spastic quadriparesis that can progress to coma and death if uncorrected. Previously known as central pontine myelinolysis (CPM) when described for the first time in 1959, it was thought to be a sequela of alcoholism or malnutrition. In the early 1980s, rapid correction of hyponatremia was established as the cause. The presumptive underlying pathophysiology is damage to the blood–brain barrier and changes in cellular volume as a response to rapid alteration in extracellular fluid osmolality, leading to loss of myelin sheath with relative sparing of axons and neurons and without inflammatory infiltrates [1]. It can also occur in the basal ganglia, thalami and supratentorial gray–white matter junction, whence the name extrapontine myelinolysis (EPM) [2,3].

CT scan may be nearly normal in the acute phase, with possible low attenuation seen in the subacute and chronic phases. On MRI, confluent hyperintense T2 and FLAIR signal can be seen (Fig. 21.1) spreading centrifugally from the median raphe, located in the dorsal basis pontis with relative sparing of tegmentum, corticospinal, and corticobulbar tracts, except in the most severe cases [2,4]. Contrast enhancement is occasionally seen in the subacute to late stages.